BACKGROUND/AIMS: Lamivudine use in patients with decompensated cirrhosis B has been reported to improve the hepatic function and often delay the need for liver transplantation. In the present study, we evaluated the efficacy and safety of long-term lamivudine therapy in patients with decompensated cirrhosis by comparative study using a matched, untreated cohort. METHODS: 41 patients with decompensated cirrhosis B were included for this study (31 male and 10 female; mean age, 50 years; mean observation period, 18 months). They were divided into two groups: a lamivudine treatment group and an untreated control group. 21 patients in the treatment group were treated with lamivudine 75 or 150 mg daily for at least 12 months. Biochemical and serologic markers were evaluated at two to three-month intervals for all patients. Clinical improvement was defined by a decrease in the Child-Pugh score of at least 2 points. RESULTS: During the observation period, 62% (13/21) was responders, 33% (7/21) was breakthrough, and 5% (1/21) was non-responder in the treated group. The mean Child-Pugh score was significantly improved from 8.6 to 6.0 in the treatment group, but aggravated from 8.7 to 10.0 in the control group during the follow-up. The HBeAg seroconversion rate was 31% in the treatment group (5/16) and none in the control group (0/14). Clinical improvement was observed in fifteen of 21 in the treatment group (71%) and only one of 20 in the control group (5%). According to the treatment responses, clinical improvement was observed in ten of 13 responders (77%), four of 7 breakthrough (57%), and one non-responder. CONCLUSIONS: The long-term administration of lamivudine for patients with decompensated cirrhosis B is effective and safe, although breakthrough and non-response occurred in some patients.
BACKGROUND/AIMS: Lamivudine use in patients with decompensated cirrhosis B has been reported to improve the hepatic function and often delay the need for liver transplantation. In the present study, we evaluated the efficacy and safety of long-term lamivudine therapy in patients with decompensated cirrhosis by comparative study using a matched, untreated cohort. METHODS: 41 patients with decompensated cirrhosis B were included for this study (31 male and 10 female; mean age, 50 years; mean observation period, 18 months). They were divided into two groups: a lamivudine treatment group and an untreated control group. 21 patients in the treatment group were treated with lamivudine 75 or 150 mg daily for at least 12 months. Biochemical and serologic markers were evaluated at two to three-month intervals for all patients. Clinical improvement was defined by a decrease in the Child-Pugh score of at least 2 points. RESULTS: During the observation period, 62% (13/21) was responders, 33% (7/21) was breakthrough, and 5% (1/21) was non-responder in the treated group. The mean Child-Pugh score was significantly improved from 8.6 to 6.0 in the treatment group, but aggravated from 8.7 to 10.0 in the control group during the follow-up. The HBeAg seroconversion rate was 31% in the treatment group (5/16) and none in the control group (0/14). Clinical improvement was observed in fifteen of 21 in the treatment group (71%) and only one of 20 in the control group (5%). According to the treatment responses, clinical improvement was observed in ten of 13 responders (77%), four of 7 breakthrough (57%), and one non-responder. CONCLUSIONS: The long-term administration of lamivudine for patients with decompensated cirrhosis B is effective and safe, although breakthrough and non-response occurred in some patients.